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Gut · Immune · Metabolic · Diagram

The Gut-Immune Interface — Three Tests, One System

How microbiome, gut barrier, food immune responses and systemic inflammation are usually drawn as one chain — and how much evidence sits behind each arrow.

Clinical diagramEvidence gradedUpdated 29 September 2026
Each arrow is graded:Strong trial or consistent human evidence Mixed some human evidence, inconsistent Mechanistic plausible mechanism, mostly animal or lab Weak / against little support, or evidence against
Start

The gut microbiome

Which organisms are present, and in what amounts. A stool PCR panel measures a selected set of organisms, including pathogens, parasites and H. pylori. It does not measure the whole microbiome, and the “normal” ranges for commensal bacteria are set by the laboratory, not by outcomes.

GI-MAP: pathogens, H. pylori, selected commensals

Mixed Microbiome → barrier. Strong for infection: gut infections clearly damage the lining. For “dysbiosis” in general, the link rests on association and animal work.
Middle

The mucosal barrier

The gut lining and the immune layer on it. Calprotectin is well validated for gut inflammation, and NICE uses it to separate inflammatory bowel disease from IBS. Secretory IgA is a real mucosal antibody, but single stool readings are hard to interpret. Serum zonulin is the weak point: a 2019 study found two widely used commercial assays were not detecting zonulin at all.

GI-MAP: calprotectin, sIgA · Blood: zonulin (read with caution)

Weak / against Barrier → food IgG → symptoms. This is the link most often drawn and least supported. Food-specific IgG mostly reflects which foods someone eats. The European allergy academy advises against IgG food testing for intolerance. The exception is coeliac disease, where the gluten–immune link is established and tested with tTG-IgA on standard bloods.
Middle

Food immune response

A food panel can prompt a supervised elimination and reintroduction. The reintroduction is the test that means something; the panel is not a list of foods to cut. If coeliac disease is possible, it has to be tested before gluten is removed, or the result is falsely reassuring.

IgG food panel (weak evidence) · Coeliac serology tTG-IgA (strong)

Mechanistic Barrier → systemic inflammation. Bacterial endotoxin (LPS) crossing a leaky barrier and driving low-grade inflammation is plausible and shown in mice. In people it is mostly associations.
End

Systemic and metabolic effects

Raised hs-CRP and changes in organic acid markers. Some organic acids produced by gut microbes (for example, arabinose and HPHPA) are reported as dysbiosis markers, but their ranges come from the testing laboratory and have little outcome validation.

Blood: hs-CRP · OAT: microbial organic acids (limited validation)

How to read this. The three tests look at one system from different sides. The chain between them is a working hypothesis: strong at some links (infection, calprotectin, coeliac disease) and weak at others (zonulin, food IgG). The honest way to use it is to treat what is documented, then check whether symptoms change.

Read the full picture

The permeability article goes through what can and cannot be measured.

Read: Intestinal permeability

Sources

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